12
Weight Loss — If You’re Overweight
Weight loss can significantly reduce your insulin resistance. You may recall from Chapter 1 that
obesity, especially abdominal (truncal, or visceral) obesity, causes insulin resistance and thereby
can play a major role in the development of both impaired glucose tolerance and type 2 diabetes.
If you have type 2 diabetes and are overweight, it is important that weight loss become a goal of
your treatment plan. Weight reduction can also slow down the process of beta cell burnout by
making your tissues more sensitive to the insulin you still produce, allowing you to require (and
therefore to produce or inject) less insulin.
It may even be possible, under certain circumstances, to completely reverse your glucose
intolerance. Long before I studied medicine, I had a friend, Howie, who gained about 100 pounds
over the course of a few years. He developed type 2 diabetes and had to take a large amount of
insulin (100 units daily) to keep it under control. His physician pointed out to him the likely
connection between his diabetes and his obesity. To my amazement, during the following year,
he was able to lose 100 pounds. At the end of the year, he had normal glucose tolerance, no
need for insulin, and a new wardrobe. This kind of success may only be possible if the diabetes is
of short duration, but it is certainly worth keeping in mind—weight loss can sometimes work
miracles.
Before we discuss weight loss, it makes sense to consider obesity, because if you don’t
understand why and how you are overweight or obese, it will be somewhat more difficult to
reverse the condition.
THE THRIFTY GENOTYPE
When I see a very overweight person, I don’t think, “He ought to control his eating.” I think, “He
has the thrifty genotype.” What is the thrifty genotype?
The hypothesis for the thrifty genotype was first proposed by the anthropologist James V. Neel in
1962 to explain the high incidence of obesity and type 2 diabetes among the Pima Indians of the
southwestern United States. Evidence for a genetic determinant of obesity has increased over the
years. Photographs of the Pimas from a century ago show a lean and wiry people. They did not
know what obesity was and in fact had no word for it in their vocabulary. Their food supply
diminished in the early part of the twentieth century, something that had occurred repeatedly
throughout their history. Now, however, they weren’t faced with famine. The Bureau of Indian
Affairs provided them with flour and corn, and an astonishing thing happened. These lean and
wiry people developed an astronomical incidence of obesity—100 percent of adult Pima Indians
today are grossly obese, with a staggering incidence of diabetes. Fully 65 percent of adults are
type 2 diabetics. Since the publication of the first edition of this book, even many Pima children
have become obese, type 2 diabetic teenagers. A similar scenario is now playing out across
the United States in the general population. The pace may be slower, but the result is similar.
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com
What happened to the Pimas? How did such apparently hardy and fit people become so grossly
obese? Though their society was at least in part agrarian, they lived in the desert, where drought
was frequent and harvests could easily fail. During periods of famine, those of their forebears
whose bodies were not thrifty or capable of storing enough energy to survive without food died
out. Those who survived were those who could survive long periods without food. How did they
do it? Although it may be simplifying somewhat, the mechanism essentially works like this: Those
who naturally craved carbohydrate and consumed it whenever it was available, even if they
weren’t hungry, would have made more insulin and thereby stored more fat. Add to this the
additional mechanism of the high insulin levels caused by inherited insulin resistance, and serum
insulin levels would have become great enough to induce fat storage sufficient to enable them to
live through famines. (See Figure 1-1.) Truly survival of the fittest— provided famines would
continue.
A strain of chronically obese mice created in the early 1950s demonstrates quite vividly how
valuable thrifty genes can be in famine. When these mice are allowed an unlimited food supply,
they balloon and add as much as half again the body weight of normal mice. Yet deprived of
food, these mice can survive 40 days, versus 7–10 days for normal mice.
Recent research on these chronically obese mice provides some tantalizingly direct evidence of
the effect a thrifty genotype can have upon physiology. In normal mice, a hormone called leptin is
produced in the fat cells (also a hormone human fat cells produce, with apparently similar effect).
The hormone tends to inhibit overeating, speed metabolism, and act as a modulator of body fat. A
genetic “flaw” causes the obese mice to make a less effective form of leptin. In recent
experiments, when injected with the real thing they almost instantly slimmed down. Not only did
they eat less but they lost as much as 40 percent of their body weight, their metabolism sped up,
and they became much more active. Many were diabetic, but their loss of weight (and the change
in the ratio of fat to lean body mass) reversed or even “cured” their diabetes. Normal mice
injected with leptin also ate less, became more active, and lost weight, though not as much.
Research on humans has not advanced sufficiently to provide conclusive evidence that the
mechanism is the same in obese humans, but researchers believe it is at least equivalent and
probably related to more than one gene, and to different gene clusters in different populations.
In a full-blown famine, the Pima Indian’s ability to survive long enough to find food is nothing short
of a blessing. But when satisfying carbohydrate craving is suddenly just a matter of going to the
grocery or making fried bread, what was once an asset becomes a very serious liability.
Although current statistics estimate slightly more than 60 percent of the overall population of the
United States as chronically overweight, there is even greater reason to be concerned, because
the number has been increasing by 1 percent each year. Some researchers attribute rising
obesity in the United States at least in part to increasing numbers of former smokers. Others
attribute it to the recent increase in carbohydrate consumption by those trying to avoid dietary
fat. Whatever the reasons, overweight and obesity can lead to diabetes. The thrifty genotype has
its most dramatic appearance in isolated populations like the Pimas, which have recently been
exposed to an unlimited food supply after millennia of intermittent famine. The Fiji Islanders, for
example, were another lean, wiry people, accustomed to the rigors of paddling out against the
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com
Pacific to fish. Their diet, high in protein and low in carbohydrate, suited them perfectly. After the
onset of the tourist economy that followed World War II, their diet changed to our highcarbohydrate western diet, and they too began (and continue) to suffer from a high incidence of
obesity and type 2 diabetes.
The same is true of the Australian Aborigines after the Aboriginal Service began to provide them
with grain. Ditto for South African blacks who migrated from the bush into the big cities.
Interestingly, a study that paid obese, diabetic South African blacks to go back to the countryside
and return to their traditional high-protein, low-carbohydrate diet found that they experienced
dramatic weight loss and regression of their diabetes.
It’s clear that thrifty genotypes work in isolated populations to make metabolism supremely
energy-efficient, but what happens when the populations have unrestricted access to highcarbohydrate foods? It would appear that the mechanism of the thrifty genotype works something
like this: Certain areas of the brain associated with satiety—that sensation of being physically and
emotionally satisfied by the last meal—may have lower levels of certain brain chemicals known
as neurotransmitters. A number of years ago, Drs. Richard and Judith Wurtman at the
Massachusetts Institute of Technology (MIT) discovered that the level of the neurotransmitter
serotonin is raised in certain parts of the hypothalamus of the animal brain when the animal eats
carbohydrate, especially fast-acting concentrated carbohydrate like bread. Serotonin is a
neurotransmitter that seems to reduce anxiety as it produces satiety. Other neurotransmitters
such as dopamine, norepinephrine, and endorphins can also affect our feelings of satiety and
anxiety. There are now more than one hundred known neurotransmitters, and many more of them
may affect mood in response to food in ways that are just beginning to be researched and
understood.
In persons with the thrifty genotype, deficiencies of these neurotransmitters (or diminished
sensitivity to them in the brain) causes both a feeling of hunger and a mild dysphoria—often a
sensation of anxiety, the opposite of euphoria. Eating carbohydrates temporarily causes the
individual to feel not only less hungry but also more at ease. A frequent television sitcom scenario
is the woman just dumped by her boyfriend who plops down on the couch with a pie or half a
gallon of ice cream, a spoon, and the intention of eating the whole thing. She’s not really hungry.
She’s depressed and trying to make herself feel better. She’s indulging herself, we think,
rewarding herself in a way for enduring one of life’s traumas, and we laugh because we
understand the feeling. But there is a very real biochemical mechanism at work here. She craves
the sugar in the pie or the ice cream not because she’s hungry but because she knows,
consciously or not, that it really will make her feel better. Contrary to popular belief, the fat in the
ice cream or in the crust of the pie doesn’t make much of a difference. It’s the carbohydrate that
will increase the level of certain neurotransmitters in her brain and make her feel better
temporarily. The side effect of the carbohydrate is that it also causes her blood sugar to rise and
her body to make more insulin; and, as she sits on the couch, the elevation in her serum insulin
level will facilitate the storage of fat.
On television the actress may never get fat. But for the real-life woman, high serum insulin levels
from eating high-carbohydrate foods will cause her to crave carbohydrate again. If she is a type 1
diabetic making no insulin, she’ll have to inject a lot of insulin to get her blood sugar down, with
the same effect—more carbohydrate craving and building up of fat reserves.
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com
GETTING IT OFF AND KEEPING IT OFF
There may be many mechanisms by which the thrifty genotype can cause obesity. The most
common overt cause of obesity is over eating carbohydrate, usually over a period of years.
Unfortunately, this can be a very difficult type of obesity to treat.
If you’re overweight, you’re probably unhappy with your appearance, and no less with your high
blood sugars. Perhaps in the past you’ve tried to follow a restricted diet, without success.
Generally, overeating follows two patterns, and frequently they overlap. First is overeating at
meals. Second is normal eating at mealtime but with episodic “grazing. ”Grazing can be anything
from nibbling and snacking between meals to eating everything that does not walk away. Many
of the people who follow our low-carbohydrate diet find that their carbohydrate craving ceases
almost immediately, possibly because of a reduction in their serum insulin levels. The addition of
strenuous exercise sometimes enhances this effect. Unfortunately, these interventions don’t work
for everyone.
Medications
If you’re a compulsive overeater, if you just can’t stop yourself from eating, and are addicted to
carbohydrate, you may not be able to adhere to our diet without some sort of medical intervention
(see Chapter 13). Carbohydrate addiction is just as real as drug addiction, and in the case of the
diabetic, it can likewise have disastrous results. (In actual fact, excess body weight kills more
Americans annually from its related complications than all drugs of abuse combined, including
alcohol.) You need not despair of never losing weight, however. I have seen a number of “dietproof” patients over the years get their weight down and blood sugars under control. Over the last
several years, medical science has gained a much more sophisticated understanding of the
interactions of brain chemicals (neurotransmitters) that contribute to emotional states such as
hunger and mood. Many relatively benign medications have been successfully applied to the
temporary treatment of compulsive overeating. There is no doubt that when used properly, many
appetite suppressants are quite effective in helping people to lose weight. If you simply cannot
lose weight, it may be helpful to discuss with your physician medicines that may be of use to you.
I have used more than 100 different medications with my patients and have found many of them
to be of great value for treating carbohydrate addiction.
There is, however, a catch to this method. Over the years, I have found that none of these
medications works continually for more than a few weeks to a few months at a time, a fact that
many if not most medical and diet professionals may be unaware of.
I developed a reasonably successful method for prolonging effectiveness of some by rotating
them weekly, so that from one week to the next a different neurotransmitter would be called into
action to provide the sensation of satiety. I found that about eight different medications, changed
every week for eight weeks, and then repeating the cycle, would perpetuate the effect for as long
as people continued to take them. At one point this looked to be a very promising means to help
get weight off and keep it off. I even acquired a patent for the technique. Over time, however, I
found several significant reasons not to continue pursuing this route. The most insurmountable of
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com
these was that it was just too difficult for most people to follow their normal regimen of diabetes
medications while at the same time changing their regimen of appetite suppressants from week to
week. Add to that the difficulty of working with a patient over a number of weeks just to find eight
medications that worked for them and could be rotated. What I did discover during all this trial and
error were two effective methods of curbing overeating. The results my patients have had with
them are so significant that I’ve devoted the whole next chapter to them.
Reducing Serum Insulin Levels
Another group of type 2 diabetics has a common story: “I was never fat until after my doctor
started me on insulin.” Usually these people have been following high-carbohydrate diets and so
must inject large doses of insulin to effect a modicum of blood sugar control.
Insulin, remember, is the principal fat-building hormone of the body. Although a type 2 diabetic
may be resistant to insulin-facilitated glucose transport (from blood to tissues), that resistance
doesn’t diminish insulin’s capacity for fat-building. In other words, insulin can be great at making
you fat even though it may be, for those with insulin resistance, inefficient at lowering your blood
sugar. Since excess insulin causes insulin resistance, the more you take, the more you’ll need,
and the fatter you’ll get. This is not an argument against the use of insulin; rather it supports our
conclusion that high levels of dietary carbohydrate—which, in turn, require large amounts of
insulin— usually make blood sugar control (and weight reduction) impossible. I have witnessed,
over and over, dramatic weight loss and blood sugar improvement in people who have merely
been shown how to reduce their carbohydrate intake and therefore their insulin doses. Although
this is contrary to common teaching, you need only visit the reader reviews of the original edition
of this book to read the similar experiences of many readers.*
Several oral insulin-sensitizing agents, which we will discuss in detail in Chapter 15, can also be
valuable tools for facilitating weight loss. They work by making the body’s tissues more sensitive
to the blood sugar–lowering effect of injected or self-made insulin. As it then takes less insulin to
accomplish our goal of blood sugar normalization, you’ll have less of this fat-building hormone
circulating in your body. I have patients using these medications who are not diabetic, and they
work in a similar way: the body is more sensitive to insulin, so it needs to produce less, and there
is, again, less of it present to build fat. One may also have less of a sense of hunger, and less
loss of self-control.
*At www.amazon.com and www.diabetes-book.com.
Increasing Muscle Mass
The above suggests what we have been advocating all along—a low carbohydrate diet. But what
do you do if this plus one of the above medications does not result in significant weight loss?
Another step is muscle-building exercise (Chapter 14). This is of value in weight reduction for
several reasons. Increasing lean body weight (muscle mass) upgrades insulin sensitivity,
enhancing glucose transport and reducing insulin requirements for blood sugar normalization.
Lower insulin levels facilitate loss of stored fat. Chemicals produced during exercise (endorphins)
tend to reduce appetite, as do lower serum insulin levels. People who have seen results from
exercise tend to invest more effort in looking even better (e.g., by not overeating, and perhaps
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com
exercising more). They know it can be done.
HOW TO ESTIMATE YOUR REAL FOOD REQUIREMENTS
Now suppose you have been following our low-carbohydrate diet, have been conscientiously
“pumping iron,” and are, in effect, “doing everything right. “What else can you do if you have not
lost weight? Well, everyone has some level of caloric intake below which they will lose weight.
Unfortunately, the “standard” formulas and tables commonly used by nutritionists set forth caloric
guidelines for theoretical individuals of a certain age, height, and sex, but not for real people like
us. The only way to find out how much food you need in order to maintain, gain, or lose weight is
by experiment. Here is an experimental plan that your physician may find useful. This method
usually works, and without counting calories.
Begin by setting an initial target weight and a reasonable time frame in which to achieve it. Using
standard tables of “ideal body weight” is of little value, simply because they give a very wide
target range. This is because some people have more muscle and bone mass for a given
height than others. The high end of the ideal weight for a given height on the Metropolitan Life
Insurance Company’s table is 30 percent greater than the low end for the same height.
Instead, estimate your target weight by looking at your body in the mirror after weighing yourself.
(It pays to do this in the presence of your health care provider, because he/she probably has
more experience in estimating the weight of your body fat.) If you can grab handfuls of fat at the
underside of your upper arms, around your thighs, around your waist, or over your belly, it is
pretty clear that your body is set for the next famine. Your estimate at this point need not be
terribly precise, because as you lose weight your target weight can be re estimated. Say, for
example, that you weigh 200 pounds. You and your physician may agree that a reasonable target
would be 150 pounds. By the time you reach 160 pounds, however, you may have lost your
visible excess fat—so settle for 160 pounds. Alternatively, if you still have fat around your belly
when you get down to 150 pounds, it won’t hurt to shoot for 145 or 140 as your next target, before
making another visual evaluation. Gradually you home in on your eventual target, using smaller
and smaller steps.
Once your initial target weight has been agreed upon, a time frame for losing the weight should
be established. Again, this need not be utterly precise. It’s important, however, not to “crash diet.”
This may cause a yo-yo effect by slowing your metabolism and making it difficult to keep off the
lost bulk. Bear in mind that if you starve yourself and lose 10 pounds without adequate dietary
protein and an accompanying exercise regimen, you may lose 5 pounds of fat and 5 pounds
of muscle. If you gain back that 10 pounds from eating carbohydrate and still are not exercising, it
may be all fat. After crash dieting, once you’ve reached your target, you may go right back to
overeating. I like to have my patients follow a gradual weight-reduction diet that matches as
closely as possible what they’ll probably be eating after the target has been reached. In other
words, once your weight has leveled off at your target, you stay on the same diet you followed
while losing weight—provided, of course, that you don’t continue losing weight. This way you’ve
gotten into the habit of eating a certain amount, and you stick to this amount, more or less, for life.
To achieve this, weight loss must be gradual. If you are targeted to lose 25 pounds or less, I
suggest a reduction of 1 pound per week. If you’re heavier, you may try for 2 pounds per week. If
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com
just cutting the carbohydrate results in a more rapid weight loss, don’t worry—just enjoy your luck.
This has happened to a number of my patients. Weigh yourself once weekly—stripped, if
possible, on the same scale, and before breakfast. Pick a convenient day, and weigh yourself on
the same day each week at the same time of day. It’s counterproductive and not very informative
to weigh yourself more often. Small, normal variations in body weight occur from day to day and
can be frustrating if you misinterpret them. Generally speaking, you won’t lose or gain a pound of
body fat in a day. Continue on your low-carbohydrate diet, with enough protein foods to keep you
comfortable.
Let’s say that your goal is to lose 1 pound every week. Weigh yourself after one week. If you’ve
lost the weight, don’t change anything. If you haven’t lost the pound, reduce the protein at any
one meal by one third. For example, if you’ve been eating 6 ounces of fish or meat at dinner, cut
it to 4 ounces. You can pick which meal to cut. Check your weight one week later. If you have lost
a pound, don’t change anything. If you haven’t, cut the protein at another meal by one-third. If you
haven’t lost the pound in the subsequent week, cut the protein by one third in the one remaining
meal. Keep doing this, week by week, until you are losing at the target rate. Never add back any
protein that you have cut out, even if you subsequently lose 2 or 3 pounds in a week.*
If you’ve managed to lose at least 1 pound weekly for many weeks but then your weight levels off,
this is a good time for your physician to prescribe the special insulin resistance–lowering agents
described in Chapter 15. Alternatively you can just start cutting protein again. Continue this until
you reach your initial target or until your visual evaluation of excess body fat tells you that further
weight loss isn’t necessary. The average non pregnant, sedentary adult with an ideal body weight
of 150 pounds requires about 9 ounces of high-quality protein food (i.e., 54 grams of pure protein)
daily to prevent protein malnutrition. It is therefore unwise to cut your protein intake much below
this level (adjusted for your own ideal body weight). If you exercise strenuously and regularly, you
may need much more than this.
Once you’ve reached your target weight, do not add back any food. You will probably have to
stay on approximately this diet for many years, but you’ll easily become accustomed to it. If you
required one of the appetite-reducing approaches described in the next chapter, do not
discontinue it.
*This may not work for girls or women with polycystic ovarian syndrome (PCOS). They may fail to lose weight
even on a near-starvation diet (see Appendix E).
SOME FINAL NOTES Reduce Diabetes Medications While Cutting Protein or Losing Weight
While you’re losing weight, keep checking blood sugars at least 4 times daily, at least 2 days a
week. If they consistently drop below your target value for even a few days, advise your physician
immediately. It will probably be necessary to reduce the doses of any blood sugar–lowering
medications you may be taking. Keeping track of your blood sugar levels as you eat less and lose
weight is essential for the prevention of excessively low blood sugars.
Increased Thrombotic Activity During Weight Loss
During weight loss, many people unknowingly experience increased clumping of the small
particles in the blood (platelets) that form clots (thrombi). This can increase the risk of heart attack
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com
or stroke. Your physician may therefore want you to take an 80 mg chewable aspirin once daily
during a meal to reduce this tendency. The aspirin should be chewed midway through a meal to
reduce the possibility of irritation to the stomach or intestines. Alternatively you can use vitamin E
in the form of gamma tocopherol or mixed tocopherols. The dosing would be 400 mg one to three
times daily depending upon your size. It need not be taken during meals, as it won’t irritate your
gastrointestinal tract.
Elevated Serum Triglycerides During Weight Loss
When you’re losing weight, fat is “mobilized” for oxidation—i.e., to be burned—and it will appear
in the bloodstream as triglycerides. If you see elevated serum triglyceride levels as you’re losing
weight, it’s not something to worry about. Your triglyceride levels will drop as soon as weight loss
levels off.
Supplemental Calcium May Help
There is recent evidence that calcium supplements (1,000–3,000 mg daily) may facilitate weight
loss by inhibiting the accompanying slowdown in metabolism that may occur when you lose
weight. As indicated previously, I recommend calcium supplements that also contain vitamin D,
magnesium, and manganese. This supplement has also been used to successfully treat the
dysphoric mood and carbohydrate craving in women who suffer from premenstrual syndrome.
Copyright ©1997, 2003 by Richard K. Bernstein, M.D.
All rights reserved. No part of this book may be reproduced in any form or by any electronic or mechanical
means, including information storage and retrieval systems, without permission in writing from the publisher,
except by a reviewer who may quote brief passages in a review.
www.diabetes-book.com